https://en.wikipedia.org/wiki/Alpha-synuclein
Knock-out mice with the targeted inactivation of the expression of alpha-synuclein show impaired spatial learning and working memory.[25] (https://en.wikipedia.org/wiki/Alpha-synuclein#cite_note-pmid22469626-25)
Full connection in next post

SB_UK

09-04-15, 09:53 AM

Sorry - long way round.

wikiP/dopamine
Outside the nervous system, dopamine functions in several parts of the body as a local chemical messenger. In the blood vessels, it inhibits norepinephrine (https://en.wikipedia.org/wiki/Norepinephrine) release and acts as a vasodilator at normal concentrations; in the kidneys, it increases sodium excretion and urine output; in the pancreas, it reduces insulin production; in the digestive system, it reduces gastrointestinal motility (https://en.wikipedia.org/wiki/Gastrointestinal_motility) and protects intestinal mucosa.^^^

I've experienced/read about ALL of the above when in ketosis ie associated with adopting ketone usage as a fuel - this is important

[quote]Supporting an instrumental role for complex I dysfunction in PD-related dopaminergic neurodegeneration, the feeding of the mitochondrial ETC directly at complex II by means of the ketone body D-β-hydroxybutyrate was shown to bypass complex I blockade, enhance oxidative phosphorylation, and attenuate dopaminergic neurodegeneration in MPTP-intoxicated mice ... ...
Mitochondria within a strong neuromelanin environment crying out to be set free.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000457
Irradiated melanin manifested a 4-fold increase in its capacity to reduce NADH

-*-

Overall, these results demonstrate that the presence of melanin contributes to the enhancement of cellular growth upon exposure to ionizing radiation in conditions of limited nutrients.

Ketosis mimics fasting.

SB_UK

09-04-15, 02:58 PM

What's going on ?

Peripheral Dopamine
and
Ketoadaptaion - using ketones as fuel

- are having the exact same effects.
In a synergistic central and peripheral way, dopamine participates in glucose homeostasis and body weight. Additionally, dopamine inhibits angiogenesis and has been shown to influence growth and apoptosis of tumoral cells. Hence, dysregulation of dopamine signaling alters cancer cell proliferation. The newly described roles of dopamine in glucose metabolism, body weight, and tumor growth should be considered in the context of chronic treatment with antipsychotic drugs influencing dopamine signaling. Additionally, dopamine-related drugs might be envisaged as new targets in the metabolic syndrome, cardiovascular diseases, diabetes, obesity, and cancer. It might be hypothesized that environmental and lifestyle changes could influence the development of diseases through readjustment of dopamine balance. Future delineation of the role of dopamine in metabolic homeostasis and cell growth might open new avenues in the prevention and treatment of obesity and cancer.
http://press.endocrine.org/doi/full/10.1210/en.2010-0745

SB_UK

09-05-15, 01:36 AM

adhd is characterized by:
https://en.wikipedia.org/wiki/alpha-synuclein
knock-out mice with the targeted inactivation of the expression of alpha-synuclein show impaired spatial learning and working memory.

so - we have repetition training intrinsic quality.
This is true for walking and building the mind.

The mind is a model of understanding which strives towards the scientific model of simplest explanatory model - making it a natural equivalent to learning to walk.

Learning to walk - movement in external space
learning to use the mind - movement in internal space.
knock-out mice with the targeted inactivation of the expression of alpha-synuclein show impaired spatial learning and working memory.12345

SB_UK

09-05-15, 01:45 AM

What drives the nerve is towards the evolutionary equivalent of parsimony/Occam's razor/simplest workable explanatory model.

In the Shawshank Redemption - appreciating freedom (The Land of the Free) was only possible following false imprisonment.

J E'S US
Passover - emergence

To uncover (realise) each of our individual Buddha natures

SB_UK

09-05-15, 02:00 AM

Melanized fungal spores are common in the sediment layers of the early Cretaceous period when many species of animals and plants died out which coincides with the Earth's crossing the “magnetic zero” resulting in the loss of its : “shield” against cosmic radiation [12] (http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000457#pone.0000457-Hulot1).

The dynamic refinement of synaptic connections is essential not only for the appropriate wiring of neural circuits, but also for behavioral responses to a changing environment as well as for learning and memory2 (http://www.nature.com/articles/srep07989#ref2). In mammalian nervous system, synapse pruning events A better understanding of the molecular mechanisms underlying synaptic pruning by microglia and its regulatory mechanisms by neuronal exosomes ...
Neuronal exosomes have also been implicated in the development of neurodegenerative diseases, as they carry several disease-related proteins such as β-amyloid, α-synuclein and TDP-43, which are involved in the pathogenesis of Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis, respectively44 (http://www.nature.com/articles/srep07989#ref44),45 (http://www.nature.com/articles/srep07989#ref45),46 (http://www.nature.com/articles/srep07989#ref46).-*-

This represents a transition in fuels within the insulin/IGF-1 to the leptin axis.
The genomic model (synonymous with quantity eg viral expansion) is meant to give way to the neural (quality) model of behaviour.

Maintain glycolysis in the CNS as learning progresses and learning is impeded.

Metabolic transition (seeded by the genomic program) is the fundamental basis upon which the generation of internal, intrinsic quality (cerebellar automatising/learning) develops.
But of course - metabolic transition isn't enough - the individual also needs to 'train'.
In places where training is possible (the classical Western World style which is found worldwide these days) - the metabolic transition is reversed ie tendency towards pro-insulin secreting diets.
In places where metabolic transition is possible (the poor/developing world style which is found worldwide also) - access to training is not afforded.
So - 2 models, sequentially arrayed - describing what it is to be human.

The genomic and neural programs
Metabolic shift from carbs to ketone usage.
The acquisition through training towards the accumulation of personal, intrinsic, innate quality.

-*-

Apparent heritability is not caused by genomic but is caused by epi-genomic variation.

... ... and so in Conclusion
ADHD [== sensitivity at empathic, systematizing and sensory levels *] represents the pained sensory overload emergence of a metabolically efficient pro-social species in an anti-social environment.

* via cortical microcircuit formation

It's all about (materialism to beauty) survival.

SB_UK

09-05-15, 03:02 AM

Cortical microcircuit formation is the mechanism by which our immersion in reality increases in resolution.
rrreality more rr{...}real

which is paraphrase of Markram's and parent to autistic children 'Intense World'.

SB_UK

09-08-15, 12:20 AM

α-Synuclein redistributes to neuromelanin lipid in the substantia nigra early in Parkinson's diseasehttp://brain.oxfordjournals.org/content/128/11/2654
The distribution and tempo of neuronal loss in Parkinson's disease correlates poorly with the characteristic and more widely spread intracellular changes associated with the disease process (Lewy bodies and Lewy neurites). To determine early intracellular changes in regions where cell loss is most marked (dopaminergic A9 substantia nigra) versus regions with Lewy bodies but where cell loss is limited, we assessed 13 patients with definite Parkinson's disease at various disease stages in comparison with controls. Using immunohistochemistry for α-synuclein, we confirmed the concentration of this protein in the soma of normal A9 neurons and in Lewy body pathology in brainstem catecholamine neurons in Parkinson's disease. Analysis of the degree of cell loss in brainstem catecholamine cell groups revealed that only the A9 substantia nigra had consistent significant cell loss early in the disease course with greater A9 cell loss correlating with increasing disease duration. To assess the earliest intracellular changes differentiating neurons more likely to degenerate, pigmented A9 and A10 neurons with and without obvious pathology were targeted, cell size and pigment density measured, and intracellular changes in α-synuclein location and lipid components analysed at both the light and electron microscope levels. There were no changes observed in healthy A10 neurons in Parkinson's disease compared with controls. Pigmented A9 neurons in later stages of degeneration with obvious Lewy body formation had a significant reduction in intracellular pigment, as previously described. In contrast, A9 neurons of normal morphological appearance and no characteristic pathology in Parkinson's disease exhibited significantly increased pigment density associated with a concentration of α-synuclein to the lipid component of the pigment and a loss of associated cholesterol. These changes in vulnerable but apparently healthy A9 neurons occurred without any change in cell size or in the amount of intracellular pigment compared with controls. The increase in pigment density is consistent with previously reported increases associated with oxidation and iron loading, reactions known to precipitate α-synuclein. The selectivity of the changes observed in A9 nigral neurons suggests that these early intracellular changes predispose these neurons to more rapid cell loss in Parkinson's disease. The increased concentration of neuronal α-synuclein and pigment in normal A9 neurons may already predispose these neurons to precipitate α-synuclein around pigment-associated lipid under oxidative conditions. Overall, these changes may trigger a cascade of events leading to larger intracellular aggregates of α-synuclein and the dispersement of protective pigment to precipitate cell death in Parkinson's disease.In sections without pre-treatment, the cytoplasm was largely devoid of α-synuclein in controls (G) with immunopositive staining and Lewy bodies observed in some of the remaining neurons in Parkinson's disease (H)http://brain.oxfordjournals.org/content/128/11/2654

-*-

What is oxidation ?
Over-working.

wildly fluctuating up <- Balance -> wildly fluctuating down

Triggered Neuromelanin a-synuclein accumulation and ... ... ...

ahhhhh!!
:D

SB_UK

09-08-15, 12:40 AM

Nerves are killed off if persistently/chronically activated.

The core mechanism of neural pruning vs neural re-arrangement.

Alpha-synuclein is specifically upregulated (https://en.wikipedia.org/wiki/Regulation_of_gene_expression) in a discrete population of presynaptic terminals of the brain during a period of acquisition-related synaptic rearrangement.[18] (https://en.wikipedia.org/wiki/Alpha-synuclein#cite_note-pmid7646890-18) It has been shown that alpha-synuclein significantly interacts with tubulin (https://en.wikipedia.org/wiki/Tubulin), ... ...

birth of a nerve cell <- re-arrangement -> death of a nerve cell

'It's like walking a high wire.'

Summarising

We need enough (synaptic re-arrangement).
But either too much or too little will trigger neural pruning loss.

Cell group A9
Group A9 is the most densely packed group of dopaminergic cells, and ... is for the most part identical with the pars compacta (https://en.wikipedia.org/wiki/Pars_compacta) of the substantia nigra ...

Densely packed - connotes importance.

The function of the dopamine neurons in the substantia nigra pars compacta (SNc) is complex.
"Dopamine neurons are activated by novel, unexpected stimuli, by primary rewards in the absence of predictive stimuli and during learning".[8] (https://en.wikipedia.org/wiki/Pars_compacta#cite_note-8) Dopamine neurons are thought to be involved in learning to predict which behaviours will lead to a reward (for example food (https://en.wikipedia.org/wiki/Food) or sex (https://en.wikipedia.org/wiki/Sex)). In particular, it is suggested that dopamine neurons fire when a reward is greater than that previously expected; a key component of many reinforcement learning models.

vs [you cannot have both the constellation of mammon AND true happiness - 'one has to choose' - the fundamental choice for man]

Succumbing to the Higher reward system -> Arraying knowledge (not disconnected knowledge, not amoral knowledge, not knowledge as pointless complexity, not knowledge is power) into understanding -> non-addictive -> since -> upon attaining wisdom, the onus (dopamine release - becomes autonomously regulated) to continue is lost

The problem with ketosis is that it's too important to require us to manage a fiddly diet.

More to follow.

MAO

http://www.pharmacology2000.com/Autonomics/Adrenergics1/fad1u.jpg

NADH2 + FADH2 - 2 KEY redox co-factors.

SB_UK

09-10-15, 02:33 AM

Coming through ... ...

Scientists have found that gut bacteria produce neurotransmitters (http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003726) such as serotonin, dopamine and GABA, all of which play a key role in mood (many antidepressants increase levels of these same compounds). http://www.theatlantic.com/health/archive/2015/06/gut-bacteria-on-the-brain/395918/

J Neurochem. (http://www.ncbi.nlm.nih.gov/pubmed/26156066#) 2015 Jul 6. doi: 10.1111/jnc.13237. [Epub ahead of print]
Norepinephrine and its metabolites are involved in the synthesis of neuromelanin derived from the locus coeruleus.

Using the chemical degradation methods for the determination of catechols in neuromelanin (NM), we have shown that dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), 3,4-dihydroxyphenylethanol (DOPE), and 3,4-dihydroxyphenylalanine (DOPA) are mainly responsible for the structure of NM from substantia nigra (SN), while norepinephrine (NE), 3,4-dihydroxymandelic acid (DOMA), and 3,4-dihydroxyphenylethylene glycol (DOPEG) are additionally responsible for the structure of NM from locus coeruleus (LC).

NE in LC ->
The locus coeruleus (\-si-ˈrü-lē-əs\, also spelled locus caeruleus or locus ceruleus[1] (https://en.wikipedia.org/wiki/Locus_coeruleus#cite_note-1)) is a nucleus (https://en.wikipedia.org/wiki/Nucleus_%28neuroanatomy%29) in the pons (https://en.wikipedia.org/wiki/Pons) (part of the brainstem) involved with physiological (https://en.wikipedia.org/wiki/Physiology) responses to stress (https://en.wikipedia.org/wiki/Stress_%28medicine%29) and panic (https://en.wikipedia.org/wiki/Panic).

-*-
Also - one can tell what's scientifically interesting - because it possesses an intrinsic interest to it; it's fun to think about.

Bad science (data accumulation) feels dull.

Also - every mechanism is in place - a beautiful clockwork mechanism where everything need work for human beings to operate.

Fatal floor of medication - you're breaking a system which is required for optimal functionality.

eg MAO required

- not to be artificially inhibited.

SB_UK

09-10-15, 07:02 AM

So - this is a turn-up for the books -
our mental health biogenic amines are simply a gut produced reagent for N scavenging towards neuromelanin polymerization towards SCFA production for biome ecosystem functioning.

Try again
[1]
https://en.wikipedia.org/wiki/Alpha-synuclein
Knock-out mice with the targeted inactivation of the expression of alpha-synuclein show impaired spatial learning and working memory.[25] (https://en.wikipedia.org/wiki/Alpha-synuclein#cite_note-pmid22469626-25)

THIS IS ADHD.

[2]
ADHD, and its core symptoms, have been associated with abnormalities in the neural systems that govern release of neurotransmitters such as dopamine and noradrenaline.[1-6]

ACCEPTED

[3]
[DOPAMINE DERIVATIVES ARE RESPONSIBLE FOR] the structure of NM from substantia nigra (SN),
while
[EPINEPHRINE DERIVATIVES ARE ALSO RESPONSIBLE] for the structure of NM from locus coeruleus (LC).

[4]
SN -> dopamine release
LC -> epinephrine release

[2]
ADHD, and its core symptoms, have been associated with abnormalities in the neural systems that govern release of neurotransmitters such as dopamine and noradrenaline.[1-6]

[6]
This key neuromodulatory system is currently thought to be critical for numerous functions including response to stress, attention, emotion, motivation, decision making and learning and memory.

[1]
https://en.wikipedia.org/wiki/Alpha-synuclein
Knock-out mice with the targeted inactivation of the expression of alpha-synuclein show impaired spatial learning and working memory.[25] (https://en.wikipedia.org/wiki/Alpha-synuclein#cite_note-pmid22469626-25)

[7]
http://www.ncbi.nlm.nih.gov/pubmed/18257649
The catecholamines play key roles in orchestrating the response to stress. While this is crucial to handle emergency situations, stress becomes maladaptive when prolonged or repeated, increasing allosteric load and susceptibility to a wide range of serious diseases.

The locus coeruleus, origin of most of the noradrenergic neurons innervating much of the brain, displays activation of additional signalling pathways and transcription factor with repeated compared to single exposure to stress.

[8]
A fundamental mechanism involved in the CNS of learning aversive and learning appetitive behaviour.
However - in the presence of chronic distress - we overload this system - and under the weight of chronic NE release - under the weight of negative re-inforcement (stick) cannot learn positive re-inforcement.

[9]
Spend our lives being chased by a stick (legal system), locked down in a meaningless life where we cannot step out of the waiting line, ... ... and so cannot develop a sense of personal quality, of a mind of rational morality.

The orthogonal standing wave model of evolution/creation - provides us with a simple model for how evolution works.

Once we're aware of that - the mind should rationalise.

When rationalised - human beings should stop killing each other for affiliation to political party, religion, football team, colour, gender etc etc - some idea of what it is to be human.

Sandwiched in between a choice of whether to adopt genomic (beat other people) vs neural (collaborate with other people) quality - where only one of these choices recruits personal quality - neural quality is strongly disease protective whereas genomic quality, beating other people - although 'rewarding' (primitive mechanism) - results in significant personal harm.

To actively choose to harm oneself, to harm other people, to damage all species, to damage the survival prospects of future generations.

-*-

To nurture personal, social/moral, rational quality
and not in any way - to assess one's worth
from position in power over any other person.

SB_UK

09-11-15, 12:33 AM

But how will people develop if they aren't forced to attend school ?

Well - if you have no co-ercion - then people will eventually get bored - remember we are hard-wired to learn.

You can't run aversive and appetitive side-by-side -
the individual and society need to choose.

All of the behaviours which we associate (and which kill children) with laziness -
fast-food, excess alcohol/cigarettes/drugs of addiction, lack of physical activity
- will not be supplied in a world freed from co-ercion (a world free of money) -

as nobody is getting paid to produce the 'food', nobody is getting paid to produce the drugs of addiction, nobody is being paid to drive you anywhere -

- gotta' do it all yourself.

Nobody in their right mind would produce harmful foods, harmful drugs or choose to drive other people around of their personal volition.

The individual HAS to do it all (and so consequently won't choose the 'wrong' option) themselves.

Jack of all trades and not a master of one which is neither here nor there.

[1] from wikiP
a-synuclein Characterization of a novel protein regulated during the critical period for [...] learning
http://www.ncbi.nlm.nih.gov/pubmed/7646890

[2] NE / Dopamine involved in Appetitive vs Aversive learning

[3] In a world which has TOO MANY rules (see legal system which is a ridiculous, massive body of rules - which nobody can ever hope to learn) - we spend our times in constant pursuit of aversive learning involving NE - excess NE production downregulates sensitivity via standard negative feedback (basic physiological mechanism) -
requiring DE / NE re-uptake inhibitors (ADHD meds) to combat sensitivity desensitized through profoundly dull insensitivity <- ADHD (disorder element) is

Summarising
CARROT not STICK by profound global societal re-arrangement in which co-ercion (money) is eliminated.
Human beings will then give human beings permission (the choice of the higher neural reward system) to become personally and collectively better.

[2]
The aromatic ring decreases the alkalinity (https://en.wikipedia.org/wiki/Base_%28chemistry%29) of the amine, depending on its substituents. The presence of an amine group strongly increases the reactivity of the aromatic ring, due to an electron-donating effect. Amines are organized into

[6]
The ratio of NAD+ to NADH inside the cell is high, while the ratio of NADP+ to NADPH is kept low. The role of NADPH is mostly anabolic reactions, where NADPH is needed as a reducing agent, the role of NADH is mostly in catabolic reactions, where NAD+ is needed as a oxidizing agent.

Summarising
There's a growth -> maintenance transition in the human life-cycle
which sees
(upon completion of growth - acquisition of wisdom - completion of mind)
- the acquisition of a post-blood glucose elevating (stimulation duality) reward strategy
- to embrace a novel reward system which pulls back the reigns on 'growth'.

Excess growth/Unregulated death without metabolic (regulated) autophagy underlies the diseases of excess immune activity, neuro-degeneration and cancer - which make up a large percentage of diseases of Western living.

SB_UK

09-11-15, 01:56 AM

Coming of age of the species

Emergent event

Imminent ?

All available information points to human beings being positioned into a place where we are able to transcend 'worldly' (food,heat,water) requirements for survival.

Not transcending the need for air though

- noting that stupid,greedy,power hungry,anti-social,psychopathic,vicious,materialistic, consumeristic,rapacious,rentier capitalist,money loving,money grabbing human beings have methods of charging people for food, heat and water - but have ABSOLUTELY no way of charging people for being outside (sun/air).

Air - all we needAir - All I Need - Extended Version (http://listenonrepeat.com/watch/?v=Hr7JuEI6qZ4&s=0&e=479#Air_-_All_I_Need_-_Extended_Version)

Gamma rays (https://en.wikipedia.org/wiki/Gamma_ray), X-rays (https://en.wikipedia.org/wiki/X-rays), and the higher ultraviolet (https://en.wikipedia.org/wiki/Vacuum_ultraviolet) part of the electromagnetic spectrum are ionizing

I love the sun.

SB_UK

09-11-15, 04:02 PM

it is interesting to note older literature reporting carbon fixation by fungi under nutrients-limited conditions (26 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677413/#R26)–28 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677413/#R28)). Fungi were reported to use CO2.
This CO2 fixation takes place in white light and leads to increase in biomass as opposed to dark fixation as part gluconeogenesis, which does not lead to a net gain of carbon. It is tempting to suggest that under limited nutrients conditions melanized fungi might use this mechanism of CO2 fixation by utilizing transduced by melanin energy of ionizing radiation instead of white light and perhaps this should be tested experimentally in future work.

previously
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677413/
This study explores the effect of continuous exposure to bright light on neuromelanin formation and dopamine neuron survival in the substantia nigra.
The rats exposed to bright light for 20 days or 90 days showed a relatively greater number of neuromelanin-positive neurons.
The rationale to investigate the effect of light on neuromelanin formation in the substantia nigra arises from evidence that dopamine in complex with iron can absorb in the visible light spectrum. Barreto et al.7 (http://www.nature.com/articles/srep01395#ref7) have shown that in the presence of Fe(NO3)3 two broad bands of dopamine absorbance appear, with maxima at 437 and 740 nm. Although light with longer wavelengths penetrates into the brain more effectively8 (http://www.nature.com/articles/srep01395#ref8), shorter wavelength light can also penetrate into deep brain structures. Gamma rays (https://en.wikipedia.org/wiki/Gamma_ray), X-rays (https://en.wikipedia.org/wiki/X-rays), and the higher ultraviolet (https://en.wikipedia.org/wiki/Vacuum_ultraviolet) part [shorter wavelength light] of the electromagnetic spectrum are ionizing

I need something like he mechanism above to set people free from a dreary materialistic low quality pointless life of worthlessness.

Little Missy

09-11-15, 04:12 PM

I need something like he mechanism above to set people free from a dreary materialistic low quality pointless life of worthlessness.

Is your life dreary, materialistic, low quality, pointless and worthless? Sometimes your posts make me so sad because you must really be suffering. :(

SB_UK

09-11-15, 10:56 PM

Do you remember all of the years that Andy was in prison in the Shawshank Redemption ?

Perhaps some events occurred of note - but overall ... ...

- his entire period in jail was working towards just one and only one outcome.

-*-

Is life in prison less than we need ?

Why is freedom (becoming free) an enduring (the aspiration to be free) mark of human evolution for thousands of years ?

Are rich people free ?

No.

Money imprisons the mind.

Who has most ?

Out in the distance her order was heard
And the soldier was killed, still waiting for her word
And while the queen went on strangling in the solitude she preferred
The battle continued on

Human beings can create wealth for themselves by supporting the suffering of others.

But all human beings will know, even if they do not acknowledge what they're doing.

And they will feel pain.

It isn't human to take advantage.

It's human to be free from dependency relationships.

The rich person that needs poor people to supply their needs is dependent.
The poor person that desires to be rich - is no different.

The poor and the needy
are selfish and greedy
in her (generally the rich) name.

The dependent (suffering dependency ie addictive -ism) never remarks that a beautiful day is enough.

SB_UK

09-11-15, 11:17 PM

And so the answer to the question - is that in the absence of freedom, whether we admit it to ourselves or not, we are not as we desire to be.

The state of freedom will associate with a global village of voluntaryism.

I can feel the mind running out of places to go.

The world of mind isn't complicated, isn't complicated at all.

We need to fire off Earth v2 and to create collective quality.

Instead of the dull, dreary, grey, nation fighting, hierarchical power -istic armed border-guard structures we have of present.

Even {insert whatever we wish to call fundamental substrate} offered us a 'choice' - not enforced a will

- a choice between rational morality (truth) and selfish greed (the illusion of comfort).

The blue and red pill.

An illusion which the mind cannot re-create once seen through.

You cannot return to the Matrix.

The Matrix concerned itself with human beings as energy generators.

That's what we really should be becoming.

Of note - the connection between the ketosis lifestyle (mimics fasting) and ... ...
under limited nutrients conditions

Why would the mind/brain/body become better unless you train them so to do ?

SB_UK

09-11-15, 11:28 PM

http://optimalprediction.com/wp/radiation-eating-fungi-they-kill-trees-and-they-kill-people/
In the original paper, the researchers Dadachova et al showed (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0000457) that ionizing radiation changes the electronic properties of melanin, and enhances the growth of melanized fungi. So any fungus species that contain melanin have their growth spurred in the presence of ionizing radiation. These are not mutant fungi, they are ordinary fungus species found everywhere in the environment. Some of them are common molds that grow in your basement or bathroom.
So these fungi do not actually feed on radiation, they change the properties of melanin, so that it can be converted into energy for growth. Think of radiation as an enzyme that allows melanin to be “digested”. Effectively, it’s the same thing, though.

That's an all-powerful basis to evolutionary selection.

The major jumps in selection - to lower eukaryotes - melanin/mitochondria in fungae
and to nervous system - melanin/mitochondria/nerve must have been driven by the re-creation of an anutonomous (like plant) radiation harvesting and utilizing biochemical framework.

So - to say that the human genome (particularly without stipulation of epigenetic modifications and effects) facilitates an understanding of man -
is incorrect.

We're agents of quality.
And quality acquisition comes through practice, experience and following one's nose into fun.

No gene for it; no medication for it; no homeopathic pill for it and no herbal product for it.
Just one societal infrastructure (capitalism) which prevents it, and one (voluntaryism) which facilitates it.
The fundamental choice between a selfish and a social reward system.

ADHD is characterized by:
Knock-out mice with the targeted inactivation of the expression of alpha-synuclein show impaired spatial learning and working memory.[25] (https://en.wikipedia.org/wiki/Alpha-synuclein#cite_note-pmid22469626-25)
https://en.wikipedia.org/wiki/Alpha-synuclein

What is a-synuclein ?

Is it bad ?
No - the genome doesn't do 'bad' - only human beings do that.

[1]Lab reagent - SDS PAGE for size denaturing proteins.
DTT is frequently used to reduce the dissulfide bonds of proteins and, more generally, to prevent intramolecular and intermolecular disulfide bonds from forming between cysteine residues of proteins.
[2]
So if DTT removes structure (quaternary
By breaking the S-S bonds, both the tertiary structure and the quaternary structure of some proteins can be disrupted
https://www.umass.edu/molvis/workshop/imgs/protein-structure2.png
to primary protein structure) then the opposite effect will be to drive pathological potentially - potentially false - quaternary structure - then a strong oxidizing (ROS) environment will trigger assembly (potentially pathological) cf taupathies/synucleopathies.

[3]
Abnormal fibrillization triggering neural degeneration.

[4]
What's the cause of ROS formation ?
Mitochondria

[5]
What's the likely basis to calming the mitochondria ?

Exceptional - to be read

This mechanism may, in part, contribute to the neuroprotective activity of ketones by restoring normal bioenergetic function in the face of oxidative stress.http://www.ncbi.nlm.nih.gov/pubmed/17240074

FULL TEXT
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865572/

SB_UK

09-12-15, 12:48 AM

Summary
The disorders of Western living are the disorders of Western style living.

the genome doesn't do 'bad' - only human beings do that.

From artificial food, to artificial human relations, to artificial work, to artificial chemicals in the water/air, to artificial material wealth, to artificial emotions, to artificial words
- it's all distressing.

And it's all done for money.

To keep people in jobs.

Why waste your life doing something that doesn't result in life becoming ever better for you ?

This life is more than just a readthrough.

Fail to contribute quality - and life upon reaching death will not have (teardrops on the fire) satisfied (http://www.urbandictionary.com/define.php?term=crying+over+spilled+milk).

The misfolding of intrinsically disordered proteins such as α-synuclein, tau and the Aβ peptide ... ...
http://www.ncbi.nlm.nih.gov/pubmed/24551051
[1]

At birth, the human brain consists of approximately 86 (± 8) billion neurons.[3][not in citation given] The infant brain will increase in size by a factor of up to 5 by adulthood. Two factors contribute to this growth: the growth of synaptic connections between neurons, and the myelination of nerve fibers; the total number of neurons, however, remains the same.[4] Pruning is influenced by environmental factors and is widely thought to represent learning.[4] After adolescence, the volume of the synaptic connections decreases again due to synaptic pruning.[4]
So
in utero neurone growth [GROWTH PHASE cf BLANK SLATE] -> postpartum neural/synaptic pruning, re-arrangement [LEARNING PERSONAL QUALITY] and circuitry 'strengthening'.

[2]
We need a mechanism of deleting neurones.

An intrinsically disordered protein - by virtue of its structure - would make the ideal 'trigger' post-oxidation and polymerization for nerve cell death.

It's a biosensor for oxidation. A fundamental part of CNS functioning.

Didn't figure on what we'dd do to it though.

--- FINALLY ---

Physiologically - why would a neurone to be deleted suffer oxidative environment over and above nerves to be maintained ?

Evidence
Too little
The selection of the pruned terminal arbors follow the "use it or lose it" principle seen in synaptic plasticity.

Too much
Desensitization through exposure to stimulus-*-

How do we maintain eustress ?

Ketogenic state with stable blood glucose level.

But but but ... ... ...
I want this entire mechanism to be autonomously regulated without the need for humans to make their usual stupid stupid interventions which mess up otherwise perfectly functional evolutionary systems.

http://www.translationalneurodegeneration.com/content/1/1/3
This review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson's disease (PD). Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation, but as an integral part of this process, superoxides and other reactive oxygen species are also produced. Excessive free radical production contributes to oxidative stress. Cells have evolved to handle such stress via various endogenous anti-oxidant proteins. One such family of proteins is the mitochondrial uncoupling proteins (UCPs), which are anion carriers located in the mitochondrial inner membrane. There are five known homologues (UCP1 to 5), of which UCP4 and 5 are predominantly expressed in neural cells. In a series of previous publications, we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium (MPP+; toxic metabolite of MPTP) and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential, and reducing oxidative stress. We also showed how their expression can be influenced by nuclear factor kappa-B (NF-κB) signaling pathway specifically in UCP4. Furthermore, we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin (hormone produced by adipocytes) acting via UCP2 against MPP+-induced toxicity. There is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with PD. Their expression, which can be induced, may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease.And :p of course

Summarising thread
There is a (the neural/collaborative/social/memomic/connectomic) reward system which concerns itself with the individual developing improved/intrinsic sensorimotor-cerebellar personal quality
- which when embraced -
safeguards human health through oxidative damage protection.

Connection to a-synuclein
In physiology - A role in neural/synaptic pruning - the key event (ie learning/synaptic+neural pruning and re-arrangement) which characterizes what it is to be human.
In pathology - Oxidative damage leads to pathological fibrillization in the naturally internally disordered proteins of tau, a-synuclein and b-amyloid.